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Comments ...

 +1  (nbme22#36)

tri-CyCliC antidepressent - anti C holinergic, C ant stand up (a1 block), C ardiotoxic (prolong qt by messing w na channels)


 +1  (nbme22#15)

Can someone explain the difference between C. (release of stored thyroid hormone from a thyroid gland infiltrated by lymphocytes) and D. (Release of thyroid hormone from a lymphomatous thyroid gland.

drdoom  @niboonsh, ending a comment with a question mark will make it appear on the "comments seeking answers" lists
nwinkelmann  A lymphomatous thyroid gland can either be due to primary thyroid lymphoma (which is almost always NHL, but is very rare) or due to Hashimoto's thyroid progression. Hashimoto's thyroiditis = lymphocytic infiltrate with germinal B cells and Hurthle cells, which upon continued stimulation, can lead to mutation/malignant transformation to B cell lymphoma. These, I believe, would still present with hypothyroidism, and thus would have low T4 and high TSH (opposite of this patient).

 +0  (nbme22#20)

I am confusion. why wouldnt this be a cross over study?

shokay  there is no washout period and the order of drugs given isn't switched

 +0  (nbme22#5)

My guess is that they are referring to Retrovirus (HIV/HTLV)- a single stranded positive sense linear RNA. Retroviruses are known to carry reverse transcriptase (RNA-dependent DNA-polymerase). The encephalitis is what threw me off cuz I automatically thought of the many negative sense RNA viruses that cause encephalitis (like arenavirus or bunyavirus). Apparently there have been a few causes of HTLV causing encephalitis... maybe this is what they were trying to get at? Idk but i just spent way too much time on this damn question https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5878187/


 +0  (nbme22#19)

https://www.ncbi.nlm.nih.gov/pubmed/15599631 The horseshoe kidney was detected before surgery in 12 patients (80%) by ultrasonography, angiography, computed tomography (CT) or excretory urography. Angiography revealed multiple or anomalous renal arteries in 8 of 12 patients studied preoperatively



 +2  (nbme22#47)

This is a case of acute transplant rejection. weeks to months after the transplant, recipient cd8 and/or cd4 t cells are activated against the donor (a type 4 HSR) and the donor starts making antibodies against the transplant. This presents as a vasculitis with dense interstitial lymphocytic infiltrates. (FA2018 pg 119)

ls3076  Actually was confused about this due to a UW explanation. UW said acute txp rejection has two types - humoral and humoral and cellular. Humoral has Neutrophilic infiltrate + necrotizing vasculitis while cellular has lymphocytosis. Can anyone simplify/explain this please?

 +0  (nbme21#34)

The obliques do the opposite action of their name. Inferior oblique moves the eye UP and OUT (extortion, elevation, ABduction). Since the question says that there is a fracture involving the orbital floor, that automatically rules out D (medial rectus and inferior oblique), leaving the only logical answer to be the inferior rectus and inferior oblique. https://www.youtube.com/watch?v=lWKkHWWDIEI

aishu007  hi, but inferior oblique moves up and in and not out

 +3  (nbme21#26)

i think of this as ole farmer joe on his actinic farm picking karats (carrots) (actinic keratosis)


 +0  (nbme21#32)

my understanding of this is from pathoma - Interstitial (atypical) pneumonia - caused by diffuse interstitial infiltrates. Can be caused by Mycoplasma pneumo, RSV, chlamydia pneumo, influenza, coxiella burentii


 +2  (nbme21#40)

SWIM

phase one - is it Safe?

phase 2 - does it Work?

phase 3 - any Improvements?

phase 4 - stay on the Market?


 +0  (nbme21#38)

i got this question right but why couldnt it be ginko biloba?

nor16  and why no therapy, i.e. cognitive training`

 +3  (nbme21#35)

this was a dumb question. the mneumonic "DIDanosine causes pancreaDIDis" is useful here


 +8  (nbme21#45)

https://www.youtube.com/watch?v=4-DuvwoH2zQ if ur lazy like me, this is a good refresher video

d_holles  Amazing video dude. Somehow never learned this in neuro lol.

 +1  (nbme20#17)

" Other classes of medications that cause hyperprolactinemia include antidepressants, antihypertensive agents, and drugs that increase bowel motility. Hyperprolactinemia caused by medications is commonly symptomatic, causing galactorrhea, menstrual disturbance, and impotence. It is Important to ensure that hyperprolactinemia in an Individual patient is due to medication and not to a structural lesion in the hypothalamic/pituitary area; this can be accomplished by (1) stopping the medication temporarily to determine whether prolactin levels return to normal, (2) switching to a medication that does not cause hyperprolactinemia "

https://www.ncbi.nlm.nih.gov/pubmed/16092584

"Non-dose-dependent side effects — Although low-dose therapy seems to minimize the metabolic complications induced by a thiazide or thiazide-like diuretic, it may not necessarily eliminate other side effects. As an example, as many as 25 percent of men treated with 25 mg/day of chlorthalidone develop a decline in sexual function [34]. Sleep disturbances can also occur, particularly if the patient is on a low-sodium diet [34]. How these problems occur is not known."

https://www.uptodate.com/contents/use-of-thiazide-diuretics-in-patients-with-primary-essential-hypertension#H2250530998


 +2  (nbme20#47)

https://www.youtube.com/watch?v=WGWFFN01qkA succinylcholine usually has v fast duration of action bcuz metabolized by plasma pseudocholinesterase. With atypical pseudocholinesterase, decreased metabolism of succinylcholine and thus causes a prolonged duration of action of succinylcholine ----> APNEA





Subcomments ...

It said it was fatal to males in utero, and the question asked about live born offspring. Since the males aren’t being born in the first place, I said 50% females and 0% males.

hungrybox  fuck i got baited +5  
jcrll  "live-born offspring" ← baited +2  
sympathetikey  Same :/ +  
arkmoses  smh +  
niboonsh  why is it 50% females tho? +  
imgdoc  felt like an idiot after i figured out why i got this wrong. +  
temmy  oh shit! +  


submitted by drdoom(163),

Calculations for dad. The probability of the father being a carrier is 2/3 since it is known that he doesn’t have the disease. Then the probability of him passing it on to his kid is 1/2, thus:

  • Probability of dad being carrier = 2/3
  • Probability of dad passing on disease allele = 1/2

Calculations for mom. With the Hardy-Weinberg Principle, you can figure out the probability of the mother being a carrier:

q = sqrt(1/40,000) = 1/200

So, 2pq = 2 * 1/200 * 199/200, which is approx 1/100.

For the child to get the allele from mom, two things need to happen: (1) mom must be a carrier [“heterozygote”] and (2) mom must pass the allele to child:

  • Probability of mom being carrier = 1/100
  • Probability of mom passing on disease allele = 1/2

Puting it all together. Now, combine all together:

= (probability of dad being carrier) * (probability of dad passing on disease allele) * (probability of mom being carrier) * (probability of mom passing on disease allele)

= 2/3 * 1/2 * 1/100 * 1/2
= 1 in 600

kernicterusthefrog  To quote Thorgy Thor, drag queen: "ew, Jesus, gross" +  
niboonsh  This question makes me want to vomit +  
drdoom  lol +  


submitted by aesalmon(32),

I feel dumb for asking but can someone explain this? If his parents are of close to normal BMI and are concerned about his weight why would they be allowing his calorie consumption to exceed his energy expenditure? ( AKA letting the kid eat too much and not exercise enough)

meningitis  That's a modern day mystery. +  
drdoom  The prompt is only asking "what's the likely cause of obesity?" It's not that they're "allowing" him to eat more than exercise. (Few parents can monitor their kids that closely!) The prompt is only asking what's the most likely explanation for his 95th percentile weight and BMI (given that he otherwise appears normal); in the United States, the most likely explanation is eating way more than you expend. +  
niboonsh  aka 'merica #firstworldproblems +  


meningiomas count as enhancing lesions? (this comment needs to be more than 50 characters apparently.)

goldenwakosu  I think it’s because meningiomas are able to calcify (aka sometimes they have psamomma bodies). I got this question wrong too but I totally did not completely register that the tumor was in the dura (interhemispheric fissure + central sulcus). Hope that helps! +  
pipter  the only reason I got this right was because they described the tumour as being near the falx cerebri. +1  
fcambridge  Other hints include being described as round and seen in a female. Both indicative of Meningioma +2  
niboonsh  also meningiomas typically present with seizures or focal neurological signs +  




submitted by seagull(350),

out of curiosity, how may people knew this? (dont be shy to say you did or didnt?)

My poverty education didn't ingrain this in me.

johnthurtjr  I did not +  
nlkrueger  i did not lol +  
ht3  you're definitely not alone lol +  
yotsubato  no idea +  
yotsubato  And its not in FA, so fuck it IMO +  
niboonsh  i didnt +  
imnotarobotbut  Nope +  
epr94  did not +  
link981  I guessed it because the names sounded similar :D +1  
d_holles  i did not +  
yb_26  I also guessed because both words start with "glu"))) +1  
impostersyndromel1000  same as person above me. also bc arginine carbamoyl phosphate and nag are all related through urea cycle. +  
jaxx  Not a clue. This was so random. +  
wolvarien  I did not +  
ls3076  no way +  
hyperfukus  no clue +  


submitted by bubbles(25),

Has anybody found a good explanation for this histology? I genuinely have no idea what I'm looking at.

meningitis  This is common in Klinefelter.. think of the equivalent of Streaked ovaries seen in Turners. White streaks, red/pink material of hyaline, and hyperplasia of Leydig cells. Just remember: It doesn't look like normal structured testicle histology (No organized seminiferous tubules with Sertoli cells around) +3  
niboonsh  https://www.pathologyoutlines.com/topic/testisklinefelter.html these pictures are kinda similar +1  


submitted by bubbles(25),

Sorry if I'm being dense...why does this woman have diarrhea due to statins, diet, and exercise? I didn't really understand what they were asking for here to be honest.

.ooo.   I believe they were asking what the most common effect of statins, which is GI upset (including diarrhea). Rarely you can have hepatotoxicity and myopathy but neither of these are a side effect in the answer choices. Hopefully this helps! +1  
niboonsh  Theyre asking about the most common side effect of Orlistat - which is really fatty diarrhea +  


submitted by bubbles(25),

Can someone explain properly how we know that this trait follows Mendelian genetics and is autosomal recessive and furthermore how the parents were heterozygous?

I guessed a lot on this question and got lucky :(

niboonsh  Autosomal Dominant disorders usually present as defects in structural genes, where as Autosomal Recessive disorders usually present as enzyme deficiencies. P450 is an enzyme, so we are probably dealing with an autosomal recessive disorder. furthermore, the question states there was a "homozygous presence of p450.....". In autosomal recessive problemos, parents are usually heterozygous, meaning that 1/4 of their kiddos will be affected (aka homozygous), 1/2 of the kids will be carriers, and 1/4 of their kids will be unaffected. +3  
nwinkelmann  Is this how we should attack this probelm?: First clue stating endoxifen is active metabolite of Tamoxifen should make us recognize this undering first pass hepatic CYP450 metabolism? Once we know that, the fact that the metabolite is decrease suggests an enzyme defect, which is supported by patient's homozygous enzyme alleles. Then use the general rule that enzyme defects are AR whereas structural protein defects are AD inheritance patters. Once we know the pattern, think that most common transmission of AR comes from two carrier parents. So offspring alleles = 25% homozygous normal, 50% heterozygous carrier, and 25% homozygous affected, thus sister has a 25% of having the same alleles as patient (i.e. homozygous CYP450 2D6*4)? +3  
impostersyndromel1000  we had the exact same thought process, so i too am hoping this is the correct way to approach it get reasoning friend +  


submitted by meatus(1),

I'm sorry but what am I missing here... I thought the whole point of diuretics is to correct volume overload by diuresis? How would total volume be increased??

niboonsh  the question is asking what would happen to the URINARY ph, bicarb, and volume. dont worry, i misread the question too -_- +4  
link981  Also misread the question, thought about the lab volumes of the BLOOD smh +1  
hyperfukus  yooooo me too!!! this is the second NBME i did this on they purposely don't write urine on the arrow categories to mess u up i swear!!! AHHHHHH +  
medulla  missed this question for the same reason .. still pissed +  


The description of bilateral lower limb loss of vibration implies DCML damage, and the absent DTRs + Romberg seem to me to be implying that he possibly has tabes dorsalis from syphilis (or something very similar in presentation).

As for the other answers, A is wrong because his motor function is intact, B is wrong because pain and temperature deficits are not mentioned, C is wrong because it implies a specific nerve is entrapped, but he has lost bilateral sensation in his entire lower extremities

D is the trickiest, and I’m not 100% sure, but I would think radiculopathy of the anterior (ventral) roots would cause motor deficits since they carry motor efferents. You might also expect that motor dysfunction to be unilateral, since it would be unlikely to have a problem with the nerve roots on both sides. also the DCML is not located near the anterior roots of the spinal cord, so if the anterior roots were affected you really wouldn’t expect to see vibratory loss.

So basically process of elimination, I do feel like sensory neuropathy is an extremely vague answer though and I wasn’t a fan of the question.

keycompany  This is a great rationale. I would like to add on that D is wrong because Radicular Neuropathy of the anterior lumbar roots would (1) be painful [radicular neuropathy is characterized by radiating pain (hence the word “Radicular”); this patient has numbness and tingling, not pain] and (2) because the anterior lumbar roots are the motor roots and do not carry sensory innervation. This patient is having a problem with his dorsal spinal cord (not anterior/ventral). +4  
hello  Want to clarify that "radiculopathy" is not synonymous with pain. Radiculopathy can cause pain, weakness, or numbness. I think the only reason Choice D. was incorrect because it discussed the "anterior lumbar roots", which would affect motor function. +3  
niboonsh  Radiculopathy is damage to the actual nerve itself, wouldnt that make it a LMN lesion and babinski would be negative? +1  
link981  Great explanation guys +  


submitted by fuckster(-43),

[special]

niboonsh  this is disgusting. +  


yotsubato  How is that NOT posterior to middle concha? bad question +1  
sympathetikey  @yotsubato - That would have been if it was the spehnoid sinus (I got it wrong too btw) +  
niboonsh  this is a good video if u need a visual https://www.youtube.com/watch?v=mf7rY1VNy70 +1  
sahusema  Sphenoethmoidal RECESS not sphenoethmoidal SINUS +  


submitted by whossayin(2),

the question was very poorly worded in my opinion, anybody else agree?

niboonsh  yea it was a dumbass question, whoever is writing these questions is undoubtedly a crazy genius but homeboy (or homegirl...homeperson?) needs a few grammar lessons. +  
yex  I agree. We know that it is a teratogen, but how does that question directs you to think about teratogenic effects instead of something physiologic? +1  
dr_jan_itor  The questions in the NBMEs by default are reject questions. So highly selective to be awful questsions. I am recieving regular heads up that the stems on the real thing lately are like 10-12 lines long. So these questions are not anywhere near like the test. NBME has f'd us good for this particular round of practice forms. +  


Arthropod for sure, but for the record I'm pretty sure this was Chikungunya Virus. Only got this from a UWorld question as I hadn't seen it until then, but apparently the arthralgia is really bad, which is what drew me to the answer.

https://www.cdc.gov/chikungunya/index.html

meningitis  More like Zika Virus (Same a. aegypti vector) since it says she has rash associated to her bone and muscle pain. I had Zika one time (i live in Puerto Rico). Remember also dengue and Zika are Flavivirus. Dengue can cause hemolysis (hemorrhagic), and Zika is associated with Guillen Barre and fetal abnormalities. +3  
nala_ula  I'm shocked that I found a fellow puerto rican on this site! Good luck on your test! +  
namira  dont be shocked! me too! exito! +1  
niboonsh  Dengue is also known as "bone break fever" which makes me think its more likely to be dengue due to the "excruciating pains in joints and muscles". https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4242787/ +1  
dr_jan_itor  I was thinking that its Murine typhus transmitted by fleas +  


submitted by drdoom(163),

2,500 students ... but you find out during your initial screen that 500 already have the disease. So, strikeout those people. That leaves 2,000 students who don’t have the disease.

Over the course of 1 year, you discover 200 students developed the infection. Thus:

200 new cases / 2,000 people who didn’t have the disease when you started your study = 10 percent

Tricky, tricky NBME ...

sympathetikey  Ah, I see. Thank you! +  
niboonsh  Im mad at how simple this question actually is +2  
sahusema  Incidence is measured from those AT RISK. People with the disease are not considered to be at risk. So 2500 - 500 = 2000 people at-risk. Of those 2000, within one year 200 develop the disease. So 200/2000 of the at-risk population develop the disease. 20/2000 = 10% = incidence +  


submitted by nosancuck(30),

Yo dis B got NO INTERNAL FEMALE ORGANS

Why dat!???

We be lookin at someone with an SRY from dere Y chromie! Dey be a Y chromie Homie so they be makin some Testis Determinin Factor which I be sure makes some nice lil ANTI MULLERIAN FACTOR so dey aint got that Female Internal Tract u know what i be sayin

And since wimminz is da DEFAULT they stil be gettin dose pussy lips and breastes

meningitis  The above explanation is correct (disregarding the hard to read and unprofessional dialect) but just in case anyone was wondering: chromatin-negative= Just a quick way of knowing it was a boy. The term applies to the nuclei of cells in normal males as well as those in individuals with certain chromosomal abnormalities +10  
yotsubato  Turner syndrome patients are also chromatin negative as well though.... +3  
sympathetikey  I didn't know a complication post-meningitis was lack of humor. +2  
sympathetikey  Ah, didn't read the last line. Yeah, that is taking it a bit far +1  
niboonsh  yall are haters. this is the first explanation that has ever made sense to me +2  
arkmoses  https://www.youtube.com/watch?v=yuXL-3eoB-o&t=77s Interesting syndrome watching this helped me to put it into real life perspective, interesting points they have no pubic hair/body hair, they apparently also dont smell, and breast size is usually increased... +  
whoissaad  How does chormatin-negative indicate a normal cell? Isn't chormatin just condensed DNA? +1  
cienfuegos  According to this paper most individuals with Turner Syndrome are chromatin negative: "One of the initial laboratory procedures used to confirm or rule out this diagnosis involves a sex chromatin determination from a buccal smear. Cells from the lining of the mouth are stained for the presence or absence of X-chromatin or Barr bodies, which represent a portion of an inactivated X chromosome. The typical Turner’s syndrome patient, who has 45 chromosomes and only one sex chromosome (an X), has no Barr bodies and is, therefore, X-chromatin negative. This abnormal X-chromatin negative finding in the majority of Turner’s syndrome females is similar to the result found in a normal male, who also has only one X chromosome, and differs from the X-chromatin positive condition observed in the normal female, who has two X chromosomes. Occasionally, the patient with features of Turner’s syndrome is found to be X-chromatin positive." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6233891/ +  
hyperfukus  i really hate haters this is awesome! +  


submitted by mcl(167),

Per p608 in FA 2019, SRY on Y chromosome results in development of testes. DHT results in development of male external genitalia (and the prostate).

mrsmac  No sertoli cells or lack of mullerian inhibitory factor makes more sense. bc there is both male and female internal genitalia but only male external genatalia. and karyotype would show 46XY. First Aid 2018 pg. 604 - the "Sexual Differentiation" charge delineates exactly this. If it were 5areductase deficiency the child would have testicles and scrotum, which in this case is absence. Hope this makes sense. Please let me know if you disagree and why. Thanks. +  
mixmasta  I believe the tricky part is that they don't mention the status of the Male external genitalia. Pg. 605 from FA ( bottom portion) shows the external development of the Male/Female genitalia; you see DHT is need for male. Furthermore, pg. 604 (SEXUAL DIFFERENTIATION) DHT is also needed for Male external development. +  
niboonsh  My understanding of this is that the diagnosis is 5alpha reductase deficiency because the newborn has female external (aka ambiguous) with male internal (aka "male genital ducts"). According to FA, leydig cells produce testosterone, which can either stimulate the mesonephric duct to form the INTERNAL male genitals (as see in the pt). Testosterone can also be acted on by 5alpha reductase to become Dihydrotestosterone, which forms the male EXTERNAL genitalia. Since this kid has "female" genitals, but has male insides and is 46XY, id say this is a simple case of 5alpha reductase deficiency. No sertoli cells or no MIF would present as both female and male internal (because MIF typically inhibits differentiation of female internal) and male external genitalia (bcuz leydig cells are unaffected) +6  


submitted by uslme123(7),

very stupid question. The virus was inhaled -- bats hang upside when they sleep and drool. So it spreads to the brain directly from the olfactory system via retrograde transport through nerves.

niboonsh  yea, aeresol transmission via bat poop in caves +  


submitted by mcl(167),

Methionine is an essential amino acid. All others listed are not.

scalpelofthenorth  Pg 81 Tyrosine is listed as an essential AA. Should be tryptophan for those who got this wrong like me. +  
neonem  But tyrosine can come from phenylalanine, so it's not really essential right? +  
gh889  in FA2019, it is listed as Tryptophan, not Tyrosine. That was corrected. +1  
usmleuser007  Note: Tyrosine is ONLY essential with PKU in children +  
niboonsh  bro FA2018 lists tyrosine as an essential AA. They played us. +1  


submitted by calcium196(6),

Ubiquitin-mediated proteolysis is not reversibly affected by insulin. The question asks for reversible ways that insulin affects it, and ubiquitination would lead to degradation via proteases, which is not reversible. Nuclear/cytoplasmic shunting makes sense because FOXO is a transcription factor, so it can’t do its job if it is in the cytoplasm!

meningitis  Thank you for your explanation! One question: How about the serine phosphorylation? Is it answered by pure memorization that the FOXO TF is serine phosphorylated, or is it a general fact that all TF's are serine-threonine phosphorylated? +  
tsl19  I'm not sure, but it may be as simple as this: ubiquitin-mediated proteolysis is irreversible, but both N/C shuttling and phosphorylation are generally reversible processes. +  
didelphus  I also guessed that FOXO must be a part of the PI3K pathway, since insulin regulates metabolism through PI3K and the question stem specifically mentions that. Phosphorylation is a major part of that pathway, so even indirectly phosphorylation would regulate FOXO. Frustrating question. +4  
niboonsh  yes, FOXO is affected downstream of the activation of PI3K. This is a really good video that explains the whole cascade https://www.youtube.com/watch?v=ewgLd9N3s-4 +  
alexb  According to wikipedia (https://en.wikipedia.org/wiki/FOXO1) phosphorylation of FOXO1 is irreversible. This is referring to phosphorylation of serine residues on FOXO by Akt, which occurs in response to insulin. But the NBME answer suggests it's reversible. What's up? +  


Can someone please explain why can't alcohol be correct in this setting?

niboonsh  rhinorrhea is specific to withdrawal from opioids (aka heroin). Look at page 554 in FA2018 +3  
dr_jan_itor  what if the alcoholic just has a concurrent rhinovirus infection ;) +1  


tinidazole preferred due to single dose

sweetmed  or metronidazole +  
niboonsh  what would his diagnosis be tho? +  
lostweightthxnorovirus  @niboonsh Giardia I believe. the trophozoite is pictured in the problem and has a classic "shield-like" appearance. FA 2019 pg. 155 has more information and the sketchy for it was really good! +1  
nwinkelmann  Per FA, DOC for giardia = metronidazole. MOA of metronidazole = formation of toxic free radical metabolites in the bacterial cell wall that damage DNA making it bactericidal and antiprotozoal. Metro treats = GET GAP = giardia, entamoeba, trichomonas, Gardnerella, anaerobes (below diaphragm), and H. pylori (as an alternative to amoxicillin in PCN allergy). Adverse effects = disulfiram-like reaction, HA, and metallic taste. I didn't know what Tinidazole is, and found out it is of the same drug class as Metronidazole, so makes sense why it would also be used for Giardia. For the purpose of the UMSLE 1, though, I think metronidazole would be DOC (especially because tinidazole isn't in FA). +  


euthyroid sick syndrome is sometimes called "low T3 syndrome." Also you know that the patient is euthyroid because her T4 and TSH are within the reference range. She is sick.

yotsubato  This is not in FA btw. +2  
niboonsh  https://www.ncbi.nlm.nih.gov/books/NBK482219/ probably caused by her recurrent pneumonia +1  
eacv  I though in this one as a sick sinus syndrome hahaha in UW. +  


submitted by taway(6),

Just as a note for anybody else who was WTF at how 2(29/30)(30/30) = 1/15...a lot of question banks round 29/30 (or any similarly large fraction) out to 1

gh889  I think you meant 2(29/30)(1/30) just to clarify! +3  
niboonsh  i am confusion +  
arkmoses  You have to use the hardy weinberg formula (1=p^2+2qp+q^2)and p + q = 1 they basically tell you that q^2=1/900 which makes q=1/30 now you can figure out (p=1-q) so p=1-(1/30), p=29/30 then to figure out carrier you solve for 2qp, 2(29/30)(1/30)=1/15 I got it wrong cuz I forgot how to figure out p but hopefully wont happen on the real deal. +3  
garibay92  2pq= 2(29/30)(1/30).... Transform this to 2 1 1 2 1 x x = _ = ____ 1 1 30 30 15 +  
garibay92  Nevermind :/ It didn't come out as planned :( +  
garibay92  /Users/carlosgutierrez/Desktop/IMG_2423.jpg +  


In psychogenic polydipsia, serum sodium is low, and after water deprivation test, urine osmolality is increased. Urine osmolality does not increase with vasopressin injection

In nephrogenic diabetes insipidus, serum sodium is high and there is no change/mild increase in urine osmolality after water deprivation

yotsubato  This patient does not undergo a water deprivation test +3  
niboonsh  Compulsive water drinking or psychogenic polydipsia is now increasingly seen in psychiatric populations. Effects of increased water intake can lead to hyponatremia causing symptoms of nausea, vomiting, seizures, delirium and can even be life threatening if not recognized and managed early. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5579464/ +2  
missi19998  Just wondering why it in not resistance to ADH action of vasopressin +  
amarousis  because he would be hypernatremic with no ADH. can't resorb any water +1  
minhphuongpnt07  low osm/urine, low os/plasma => psychogenic polydipsia +